Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of nano-enzyme on gene expression during oxidative stress of human mesenchymal stem cells

ABSTRACT: Stem cells are severely weakened by elevated reactive oxygen species (ROS) in the inflammatory bone defect microenvironment. It is therefore of critical importance to modulate the level of extracellular ROS for the reversal of stem cell unfavorable environment. Here, we present a stable monatomic ruthenium biocatalyst anchoring on the surface of cobalt nickle layered double hydroxides (Ru-LDH) for catalytic reactive oxygen species (ROS) scavenging. We here report the changes of transcription factors human mesenchymal stem cells (hMSCs) with/without treatment with Ru-LDH under the oxidative stress condition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235884 | GEO | 2024/10/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Influence of nano-enzyme on gene expression during oxidative stress of human mesenchymal stem cells

Project description:Stem cells are severely weakened by elevated reactive oxygen species (ROS) in the inflammatory bone defect microenvironment. It is therefore of critical importance to modulate the level of extracellular ROS for the reversal of stem cell unfavorable environment. Here, we present an electron-donable heterojunction with Ru-Cu pair sites (Ru-Cu/EDHJ) for catalytic reactive oxygen species (ROS) scavenging. We here report the changes of transcription factors human mesenchymal stem cells (hMSCs) with/without treatment with Ru-Cu/EDHJ under the oxidative stress condition.

2024-09-14 | GSE253527 | GEO

Cellular and molecular response to ruthenium(II)-arene complex with substituted picolinato ligand in HeLa cells

Project description:Ruthenium(II)-arene complexes are promising drug candidates for therapy of solid tumors. We have previously shown that ruthenium(II)-arene complex [Ru(η6-p-cymene)(L7)Cl] (RuT7) exerts cytotoxic effects in a panel of cancer cell lines (J. Organomet. Chem. 2014, 749, 343–349). In this study we analyzed in vitro cellular response and performed whole-transcriptome microarray gene expression analysis in HeLa cells in order to understand the cellular and molecular mechanism of response to RuT7 complex. Results on biological action of ruthenium complex obtained on cellular level were reflected on molecular level as well. Analysis of functional categories and signaling and biochemical pathways that are associated with HeLa cells' response to ruthenium complex revealed that RuT7 complex leads HeLa cells through intrinsic (mitochondrial) apoptotic pathway, via indirect DNA damage made by action of reactive oxygen species and through direct DNA binding of RuT7. Performed molecular toxicity analysis has shown that RuT7 has fewer associated toxicity profiles than cisplatin. Altogether these results provide the basis for development of RuT7 in animal and pre-clinical studies as a potential drug candidate. We hybridized each condition (control, RuT7 and CDDP) at each time point (12 h and 24 h) in triplicate, for a total of 18 samples.

2015-09-11 | E-GEOD-72905 | biostudies-arrayexpress

Cellular and molecular response to ruthenium(II)-arene complex with substituted picolinato ligand in HeLa cells

2015-09-11 | GSE72905 | GEO

Nano gold simulated autophagy prevents cell death

Project description:We showed a kind of rectangular shaped gold-based nanoparticles (gold nanocages, GNC) could enhance the survival of cells from hydroxyurea induced cell apoptosis and significantly reduced the reactive oxygen species (ROS) levels.The nanoparticles could initiate single layer isolation membrane elongation after been phagocytosed, followed by autophagosome and autolysosome formation, then specifically integrated into the autophagosome inner membrane and bind to p62. Through recycling ribosome proteins and activate Nrf2 mediated activation of GATA3 signaling, rescue the cell death and enhanced cell and life survival.

2020-05-09 | GSE131033 | GEO

Transcription profiling of bone marrow hematopoietic stem cells and myeloid progenitors from mice with conditional deletion of Forkhead O (FoxO) family of transcription factors

Project description:To investigate the role of FoxO transcription factors as mediators of hematopoietic stem cell resistance to oxidative stress. Experiment Overall Design: Study the effect of the deficiency of FoxO1, FoxO3, and FoxO4 in murine bone marrow hematopoietic stem cells and myeloid progenitors on expression of genes involved in reactive oxygen species (ROS) metabolism.

2007-11-15 | E-GEOD-6623 | biostudies-arrayexpress

Impaired stability of tumor cells after targeting of lactate/pyruvate metabolism investigated by shotgun proteomics

Project description:Overexpression of heat shock proteins (HSPs), especially the major stress-inducible 72 kDa heat shock protein 70 (Hsp70), in malignant tumor cells is associated with therapeutic resistance. The heightened metabolic demand in tumor cells (Warburg effect) increases lactate dehydrogenase (LDH) activity and the corresponding increase in lactate concentrations promotes malignancy. Herein, we assessed the co-regulation of LDH and the heat shock response and its link to radiation resistance in B16F10 murine melanoma cells and LS174T human colorectal adenocarcinoma cells. Inhibition of LDHA/B by oxamate or GNE-140, significantly diminishes the expression of Hsp90, Hsp70 and Hsp27 in the cytosol. Diminished expression was also observed in LDHA/B double knockout (LDH-/-) cells. An increased production of reactive oxygen species (ROS) induced by a faster growth rate in wild type (WT) vs LDH-/- cells contributes to increased cytosolic HSP levels in WT cells. LDH-/- cells exhibit a lower density of membrane Hsp70 expression than WT cells and a decreased presence of the tumor-specific, Hsp70 anchoring glycosphingolipid Gb3 on the cell surface which could be attributed to an altered lipid metabolism mediated by the LDH knockout. Functionally, a double knockout of LDHA/B results in a generalized reduction in expression of HSPs in tumor cells and significantly increases radiosensitivity which is associated with a G2/M arrest. In summary, we demonstrate that pharmacological targeting of the lactate/pyruvate metabolism breaks radioresistance by impairing the stress response.

2022-02-17 | PXD026078 | Pride

New ruthenium-cyclopentadienyl complexes affect colorectal cancer hallmarks showing high therapeutic potential

Project description:Colorectal cancer (CRC) is one of the most lethal cancers worldwide. Current therapeutic strategies are accompanied by low success rates and several side effects, representing a relevant clinical problem and requiring the discovery of new and more effective therapeutic alternatives. Ruthenium drugs emerged as one of the most promising metallodrugs due to their high selectivity to cancer cells. In this work, we studied for the first time the anticancer properties and mechanisms of action of four lead Ru-cyclopentadienyl compounds, namely PMC79, PMC78, LCR134 and LCR220, in CRC-derived cell lines. Biological assays were performed in CRC cell lines to evaluate cellular distribution, colony formation, cell cycle, proliferation, apoptosis, motility as well as cytoskeleton and mitochondrial alterations. Our results showed that all compounds displayed high bioactivity and selectivity, as shown by low IC50 concentrations against CRC cells. We observed that all Ru compounds had different intracellular distributions and inhibited to a high extent the clonogenic ability and proliferation of CRC cells. In addition, PMC79, LCR134 and LCR220 induced apoptosis, increased the levels of reactive oxygen species, induced mitochondrial alterations and affected F-actin cytoskeleton organization and cellular motility. A proteomic analysis showed that these compounds induce alterations in several cellular proteins related to the phenotypic alterations induced. Overall, we demonstrated that Ru compounds, in special PMC79 and LCR220, present promising anticancer activity in CRC cells and potential to be used as new metallodrugs for CRC therapy.

2023-07-20 | PXD041324 | Pride

Mitochondrial alternative NADH dehydrogenases limit ROS, protect chloroplasts and promote survival of reoxygenation in Arabidopsis

Project description:Weather extremes are increasing worldwide frequently exposing plants to transient flooding. When floodwaters recede, plants have to cope with increased light intensity and elevated oxygen that favor excessive formation of reactive oxygen species (ROS). We report a novel molecular mechanism that helps Arabidopsis leaves cope with reoxygenation in the light that reveals a central role of the alternative electron tranport in mitochodria in cellular ROS management that is beneficial for photosynthetic recovery and provides tolerance to reoxygenation stress.

2022-12-02 | PXD032119 | JPOST Repository

MYB30 orchestras ROS wave-triggered systemic transcriptomic responses and plant acclimation in Arabidopsis

Project description:MYB30 was found to regulate reactive oxygen species (ROS) - mediated systemic transcriptomics responses to light stress in Arabidopsis

2020-08-31 | GSE141916 | GEO

Transcription profiling of liver from p38aDhep, IkkbDhep, and control mice 4h after injection of diethylnitrosamine

Project description:Analysis of microarray data from livers 4 hr after DEN administration revealed changes in the expression of several genes relevant to regulation of reactive oxygen species (ROS) accumulation, cell death, and cell cycle control.

2008-05-23 | E-TABM-351 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data